Laryngitis

clinical presentation
acute / chronic depends on:
infectious /
• cause
noninfectious
• the amount of tissue
localized / systemic
edema
inflammatory process
• the region of the
larynx primarily
involved
• patient's age.
symptoms:
Dysphonia, Odynophonia, Dysphagia,
Odynophagia, Cough, Dyspnea, stridor
 Based on the history and the laryngeal
examination
 Sometimes requires special diagnostic tests:
 cultures, blood tests, skin tests, pH monitoring,
biopsies, or radiographs
History
Gradual or sudden onset
Stridor
Associated upper respiratory infection or
heartburn•
Duration, chronicity of symptoms
Intermittent or progressive symptoms
Examination
Listen to voice, breathing
Indirect, mirror laryngoscopy
Fiberoptic assessment
Radiographic studies
Skin tests
Laboratory tests
Biopsy
In adults:
 usually less serious than in children  larger adult
larynx can accommodate swelling without
obstructing as readily.
 most commonly caused by a viral upper respiratory
infection, smoking, or laryngopharyngeal reflux
(LPR)
 CAUSA
Infectious laryngitis
Viral:commonly rhinovirus, parainfluenza;
rare cytomegalovirus, human papillomavirus,
herpes simplex virus
Bacterial:Haemophilus influenzae, streptococcus,
staphylococcus, Klebsiella
Fungal: candida, aspergillus, coccidiomycosis,
blastomycosis
Mycobacterium
Protozoa rare: leishmaniasis cryptosporidiosis
 CAUSA
Systemic diseases causing laryngitis
Wegener granulomatosis
Rheumatoid arthritis
Amyloidosis
Relapsing polychondritis
Systemic lupus erythematosus
Sarcoidosis
Epidermolysis bullosa
Cicatricial pemphigoid
 CAUSA
 Reactive laryngitis in adults
Laryngopharyngeal reflux
Smoking
Voice abuse
Inhaled steroids
Inhaled exposure : Freon, formaldehyde,
solvents
Angioedema
Allergy
Viral Laryngitis
 self-limited disease

 generalized viral syndrome and dysphonia

 voice breaks, episodic aphonia, and a lowering

of the vocal pitch
 Rhinoviruses >>

 vocal fold mucosa is erythematous and

edematous
 Treatment:
 humidification, voice rest, hydration, smoking
cessation, cough suppressants, and expectorants.
 Antibiotics : for secondary bacterial infection
Bacterial Laryngitis
 Supraglottitis = acute epiglottitis
 Aetiology:
 Haemophilus influenzae >>
 Streptococcus pneumoniae,
 Staphylococcus aureus,
 hemolytic streptococci
 Klebsiella pneumoniae
 Symptoms: fever, sore throat, muffled
voice, odynophagia, and dyspnea.
 by observing the swollen, red supraglottis by
fiberoptic laryngoscopy
 or by detecting a swollen supraglottis
(thumbprint sign) on standard lateral neck
radiographs.
 Treatment:
 Severe airway symptoms such as dyspnea, severe
stridor, or cyanosis  immediate establishment of an
airway
 less severe cases  medical management, close
observation, and serial fiberoptic examinations
 symptoms progress rapidly <24 hours / drooling (+)
airway compromise
 Medical treatment : humidification, hydration,
corticosteroids, and IV antibiotics
 Complication: Epiglottic abscess
 uncommon
 more commonly in adults than in children.
 lingual side of the epiglottis
 may be diagnosed by direct visualization or
computerized tomographic evaluation.
 Management : immediate operative airway
management followed by drainage.
Fungal Laryngitis
 often overlooked and misdiagnosed mimics
leukoplakia (clinically and histologically)
 causative organism:
 Candida
 less common: blastomyces, histoplasma, aspergillus, or
coccidioides
 histologically as pseudoepitheliomatosis hyperplasia
 susceptible to laryngeal fungal infection:
 decreased systemic immune response (diabetes,
immunosuppressive medication, nutritional deficiencies,
human immunodeficiency virus [HIV], chronic lymphocytic
leukemia
 decreased local immune response (previous radiation
therapy, inhaled cortico-steroids, LPR, smoking)
 Dx:
 Specific fungal stains: periodic acid Schiff (PAS) 
pseudohyphae and spores amid the reactive atypia
 hyperkeratosis : hematoxylin and eosin (H&E) stains

 Treatment
 noninvasive infections : oral antifungal such as
fluconazole, itraconazole, or voriconazole.
 elimination of predisposing factors.
Histoplasmosis
 Systemic mycotic disease

 Caused by Histoplasma capsulatum

 Nodular superficial granulomas that can

ulcerate and become painful
 Histologic examination : granulation tissue
composed of plasma cells; macrophages
containing the organisms; and giant cells
confused with carcinoma or tuberculosis.
 Diagnosis is made by the complement fixation
test and by culturing the organism.
 Treatment of choice: Amphotericin B
 Extensive ulceration chondritislaryngeal
stenosis.
 laser excision / tracheotomy
Blastomycosis
 caused by the fungus Blastomyces dermatitidis

 North American blastomycosis : chronic

pulmonary infection (common in the
southeastern USA)
 The organism produces small, red, granular
lesions of the laryngeal mucosa painful
abscesses and ulcerations
 Histologic examination: pseudoepitheliomatous
hyperplasia
 Similarity of the histologic H&E findings with
squamous cell carcinoma
 The PAS-positive yeast form : thick-walled
cells with broad-based buds  may be seen in
the region of the microabscesses
 Treatment : long-term amphotericin B,
ketoconazole, or itraconazole.
Tuberculosis
 most common granulomatous disease of the
larynx
 often associated with active pulmonary
tuberculosis
 Respiratory obstruction in the advanced
stages.
 Systemic complaints: fever, night sweats, and
weight loss.
 Laryngeal examination :
 diffusely edematous and hyperemic mucosa
 involving the posterior third of the larynx
 or granular exophytic lesions, which may resemble
carcinoma
 diagnosis is made by demonstrating the
organisms by smear and culture
 If tuberculous laryngitis is left untreated,
stenosis may develop, necessitating
tracheotomy.
Syphilis
 later stages of syphilis

 Diffuse erythematous papules, edema, and

ulcers mimic carcinoma along with cervical
lymphadenopathy (secondary stage)
 clear spontaneously within several weeks

 Gumma formation (tertiary stage ) fibrosis,

chondritis, and stenosis
 Treatment of choice: Penicillin
 Leprosy
 caused by Mycobacterium leprae
 most commonly involves the supraglottic larynx
 muffled voice, odynophagia, and cough
 Laryngoscopy : nodular, edematous supraglottis with
ulceration
 Diagnosis is made by biopsy chronic inflammatory
cell infiltrate with foamy cells that contain the M.
leprae bacillus
 Nasal smears for the intracellular organisms may be
diagnostic
 Treatment: long-term combination with rifampin and
dapsone. Tracheotomy may be required if stenosis
develops
 Scleroma
 chronic progressive infection caused by
Klebsiella rhinoscleromatis
 endemic to North and Central Africa, Egypt,
Central and South America, and Eastern
Europe
 primarily involves the nasal cavity, but it may
involve the laryngopharynx
 has three overlapping clinical stages
1. catarrhal stage is characterized by purulent
rhinorrhea, with nasal crusting and obstruction,
2. granulomatous stage, in which nodular
granulomas form within the upper respiratory
tract. The subglottis is most commonly
involved.
3. sclerotic stage is manifested as fibrosis and scar
formation. Dysphonia and respiratory
obstruction may develop usually takes many
years.
 diagnosis is made by isolating the organism
from the tissues or via immunohistochemical
studies
 Histologically: foamy vacuolated histiocytes
(Mikulicz cells) and degenerated plasma cells
(Russell bodies)
 Treatment : tetracycline, fluoroquinolones, or
clofazimine. Endoscopic laser resection and
tracheotomy may be required
 Wegener Granulomatosis
 systemic disease
 characterized by necrotizing granulomas with
vasculitis
 involving the respiratory tract and kidneys
 Laryngeal involvement (25%) , nasal involvement
(90%).
 initially resemble acute laryngitis 
granulomatous ulcers within the larynx
 Subglottic involvement  difficult to manage
 Diagnosis :
 histologic findings of necrotizing granulomas and
vasculitis.
 antinuclear anticytoplasmic autoantibody test (c-ANCA)
 specific (90%).
 Medical treatments: cyclophosphamide,
corticosteroids, methotrexate, and azathioprine
 Surgical treatments :
 mechanical subglottic dilation +/ - intratracheal injection
of glucocorticoids; topical application of mitomycin C;
 laser therapy
 airway obstructiontracheotomy , laryngotracheoplasty
 Rheumatoid Arthritis
 autoimmune disease
 25% of cases
 Symptoms : variable
 globus, hoarseness, stridor, and dysphagia
 first stage: active phase tender and
erythematous
 second stage :chronic phase 
 mucosa appears relatively normal
 cricoarytenoid joint is ankylosed
 submucosal nodules may be found on the true vocal
folds
 Systemic treatment : corticosteroids or other
immunosuppressive agents
 Surgical excision is performed for symptomatic
rheumatoid nodules.
 Amyloidosis
 idiopathic disorder
 characterized by the extracellular deposition of
protein leading to tissue damage, with a peak
incidence in the fifth decade.
 It often presents with laryngeal findings but
may present as a component of systemic
amyloidosis
 Clinically, the systemic type of amyloidosis can
be divided into two types:
 primary amyloidosis: associated with an
immunocyte dyscrasia such as multiple myeloma
 secondary amyloidosis: occurs as a result of an
underlying chronic inflammatory condition
 rheumatoid arthritis,
 inflammatory bowel disease,
 tuberculosis
 nonimmunocyte derived tumors : renal cell carcinoma
or Hodgkin disease
 Symptom: usually asymptomatic until the deposits
involve the vocal folds  dysphonia or they
critically narrow the airway
 Sign:
 diffuse mucosal thickening,
 submucosal nodules,
 less common: polypoid lesions.
 Clinical findings at laryngoscopy are difficult to
distinguish from other laryngeal lesions.
 Diagnosis : by pathologic examination of tissue
samples amorphous Congo red staining
material, with characteristic apple-green
birefringence (polarized light microscopy)
 Symptomatic cases : treated by endoscopic
removal of lesions.
 Systemic disease is evaluated with appropriate
immunoelectrophoretic studies.
 Life-long follow-up is important with this
condition because of its chronic and recurrent
nature.
 Relapsing Polychondritis
 episodes of inflammation and fibrosis with
destruction of the cartilage of the ears, nose,
larynx, and tracheobronchial tree.
 Laryngeal disease : more than half the cases
 manifested by dysphonia, dysphagia, and
throat pain
 Airway involvement leads to the high
mortality
 etiology : unknown
 pathogenesis : immunologic reaction to type II
collagen
 diagnosis is usually made on clinical findings
alone
 Treatment :
 milder cases : non-steroidal antiinflammatory agents,
dapsone, and colchicine.
 more severe cases: corticosteroids and other
immunosuppressive drugs such as methotrexate or
azathioprine are required in .
 Tracheotomy may be necessary.
 Systemic Lupus Erythematosus
 one-third of patients
 Symptoms range from intermittent dysphonia to
airway obstruction,
 Dysphonia and dyspnea : most common laryngeal
symptoms.
 Examination :
 edema (particularly of the supraglottis),
 ulceration,
 vocal fold paralysis.
 Most patients readily respond to systemic
corticosteroid therapy.
 Sarcoidosis
 multisystem granulomatous disease of unknown
etiology.
 diagnosis : based on finding noncaseating granulomas
and pale diffuse edema of the supraglottis
 DD: tuberculosis, Wegener granulomatosis, and fungal
disease.
 Symptoms : dysphonia and varying degrees of airway
obstruction.
 Lesions usually resolve with the use of systemic and
intralesional corticosteroids.
 Endoscopic surgery, low-dose radiation therapy, and
inhaled steroids have been used as alternative
therapies .
 Tracheotomy is rarely necessary.
 Epidermolysis Bullosa and Cicatricial
Pemphigoid
 autoimmune disorders
 manifested by mucosal blister formation .
 Bullae or ulcerations heal by scar tissue
formation.
 Involvement of the larynx is relatively
uncommon
 Symptoms : dysphonia and airway obstruction.
 Laryngeal findings : edema, raw mucosa,
bullae, ulcers, webs, and areas of stenosis in the
larynx and trachea.
 Intubation avoided if possible : larynx
sensitive to trauma.
 tracheotomy despite corticosteroid and
immunosuppressive therapy.
 Stenosis  treated by endoscopic techniques
 Laryngopharyngeal Reflux
 noninfectious laryngitis
 acute, chronic, or intermittent pattern of
laryngitis
 development of vocal fold granulomas,
laryngeal stenosis, recurrent laryngospasm,
globus pharyngeus, cervical dysphagia,
asthma, laryngeal carcinoma, and chronic
cough
 subglottic stenosis :92%
 LPR is underdiagnosed and undertreated because
its signs, symptoms, and mechanisms are
different from those seen in gastroenterology
patients:
 heartburn, regurgitation, and esophagitis.
 Examination of the larynx may reveal a variety of
findings:
 red arytenoids with interarytenoid mucosal
hypertrophy, infraglottic edema
  diffuse edema, Reinke's edema, or mucosal
thickening without significant erythema
 diffuse erythema with granular, friable mucosa, and
vocal process granulomas, with or without
associated laryngeal edema and erythema
 Diagnosis: ambulatory 24-hour double-probe
pH monitoring (current gold standard )
 Treatment :
 dietary and lifestyle modifications
 antireflux medication: proton pump inhibitors (PPI),
histamine (H2) blockers, or both
 Traumatic Laryngitis
 commonly caused by vocal abuse
 also can result from persistent coughing,
muscle tension dysphonia, or direct
endolaryngeal injury
 mucosa of the true vocal folds is hyperemic
from dilated vessels on the vocal fold surface
 edema within Reinke's space develops, and
submucosal hemorrhage may occur
 self-limited
 subsides within a few days when treated with
voice conservation and humidification
 Thermal Injury
 Exposure of the larynx to steam, smoke, or very
hot liquids or food
 Treatment : humidification, cortico-steroids,
and airway observation or intubation if the
larynx is severely edematous
 Angioedema
 inflammatory reaction
 characterized by vascular dilation and
increased vascular permeability.
 It can be caused by a variety of substances and
is potentially life threatening
 immunoglobulin E (IgE) mediated allergic
reaction
 Treatment must be aggressive.
 Supplemental oxygen, epinephrine,
corticosteroids, antihistamines, and
aminophylline are the mainstays of therapy
 If airway obstruction develops, intubation or
tracheotomy may be required.
 Allergic Laryngitis
 Symptoms : chronic and recurrent dysphonia
 Evaluation : begins with a careful history,
noting specific or chronic environmental
exposures or association of symptoms with
certain foods.
 Examination : laryngeal edema and polypoid
mucosa
 Treatment : avoidance , antihistamines,
steroids, and immunotherapy.
 Adjunctive treatment measures may include
optimizing vocal hygiene with hydration and
voice therapy to avoid pathologic
compensatory behaviors.
 Radiation Laryngitis
 Post radiation therapy for laryngeal
malignancies
 Symptoms: dysphonia, dysphagia, pain, or
globus pharyngeus
 Examination : erythematous, swollen larynx
with exudate and crusting
 Treatment involves hydration, humidification,
and acid suppression, with steroids and
antibiotics occasionally
 Laryngotracheobronchitis
 Obstructive subglottis airway
 Spasmodic / follow an upper respiratory track
infection
 Etiology:
 Viral: parainfluenza & influenza viruses, measles,
varicella
 Infection may exend from the larynx trachea,
bronchi, and bronchioles
 Symptoms:
 low-moderate fever
 RR ↑, inspiratory stridor, hoarsness, barking cough,
expiratory rhonchi respiratory distress
 Treatment:
 Hydration, humidification
 moderate to severe distress: aerozolized racemic
epinephrine ( 0.5 mL of a 2.25% sol. Diluted in 3 mL
of NS) hospital setting: rebound mucosal edema
recurrent obstruction
 mild to moderate: steroid
 Recurrent: laryngoscopy / bronchoscopy  asses
structural abnormslity.